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Titolo:
Transforming growth factor beta from multiple myeloma cells inhibits proliferation and IL-2 responsiveness in T lymphocytes
Autore:
Cook, G; Campbell, JDM; Carr, CE; Boyd, KS; Franklin, IM;
Indirizzi:
Univ Glasgow, Royal Infirm, Dept Med, ATMU, Glasgow G31 2ER, Lanark, Scotland Univ Glasgow Glasgow Lanark Scotland G31 2ER ow G31 2ER, Lanark, Scotland
Titolo Testata:
JOURNAL OF LEUKOCYTE BIOLOGY
fascicolo: 6, volume: 66, anno: 1999,
pagine: 981 - 988
SICI:
0741-5400(199912)66:6<981:TGFBFM>2.0.ZU;2-A
Fonte:
ISI
Lingua:
ENG
Soggetto:
ACTIVATION ANTIGEN CD69; MONOCLONAL GAMMOPATHIES; B-CELLS; EXPRESSION; FAS; APOPTOSIS; LIGAND; CYCLE;
Keywords:
tumor; immunity; cytokines;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
32
Recensione:
Indirizzi per estratti:
Indirizzo: Campbell, JDM Univ Glasgow, Royal Infirm, Dept Med, ATMU, Glasgow G31 2ER,Lanark, Scotland Univ Glasgow Glasgow Lanark Scotland G31 2ER nark, Scotland
Citazione:
G. Cook et al., "Transforming growth factor beta from multiple myeloma cells inhibits proliferation and IL-2 responsiveness in T lymphocytes", J LEUK BIOL, 66(6), 1999, pp. 981-988

Abstract

Multiple myeloma (MM) is a cancer of plasma cells, characterized by profound suppression of host immune responses, Here we show that MM cell lines significantly suppress the proliferation, blasting, response to interleukin-2(IL-2), and expression of CD25 by concanavalin A (Con A)activated or allostimulated peripheral blood T lymphocytes. T cells arrest iu the G1 stage ofthe cell cycle, and do not enter time IL-2 autocrine growth pathway. T tell inhibition was mediated by a soluble factor. MM cell lines did not produce IL-10 but did produce large amounts of transforming growth factor beta 1 (TGF-beta 1). T cells were assessed for their ability to respond to IL-2 when co-cultured with MM cells in the presence or absence of the TGF-beta inhibitor, TGF-beta latency-associated peptide (LAP), MM cells suppressed IL-2responses but this inhibition was completely reversed by TGF-beta LAP. A CD25(-), IL-2-dependent blast cell Line was not inhibited by MM cells or rhTGF-beta, confirming the specificity of the inhibition mechanism for the IL-2 autocrine growth pathway. We conclude that MM cells suppress T cells in their entry into the autocrine IL-2/CD25 pathway and in response to IL-2, and that TGF-beta has a significant role to play.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 20/09/20 alle ore 07:58:08